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Prepublished online as a Blood First Edition Paper on July 25, 2002; DOI 10.1182/blood-2001-11-0106. This Article Full Text (PDF) All Versions of this Article: 2001-11-0106v1 100/12/4049    most recent Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Rights and Permissions Citing Articles Citing Articles via HighWire Citing Articles via CrossRef Citing Articles via Google Scholar Google Scholar Articles by Geldhof, A. B Articles by De Baetselier, P. Search for Related Content PubMed PubMed Citation Articles by Geldhof, A. B Articles by De Baetselier, P. Social Bookmarking                   What's this? Submitted November 30, 2001 Accepted July 12, 2002 Antagonistic effect of NK cells on alternatively activated monocytes: a contribution of NK cells to CTL generation Anja B Geldhof*, Jo A Van Ginderachter, YuanQing Liu, Wim Noel, Geert Raes, and Patrick De Baetselier Laboratory of Cellular Immunology, VIB-VUB/IMOL II, St-Genesius Rode, Belgium * Corresponding author; email: abgeldho{at}vub.ac.be. NK cells fulfill essential accessory functions for the priming of antigen-specific cytotoxic T lymphocytes. Based on a NKG2D-ligand positive tumor model, we obtained results implicating NK-mediated regulatory as well as NK-mediated cytolytic activities in the initiation and persistence of CTL activity. Indeed, CD8+ T cell-dependent tumor rejection requires NK function in vivo, since tumors will progress both upon depletion of NK cells or in the absence of optimal NK activity. Here we provide evidence that the absence of NK cells during subcutaneous tumor growth will abrogate generation of anti-tumor CTL responses and that this process can be linked to the expansion of alternative activated monocytes. Indeed, our in vitro studies demonstrate that in splenic cultures from NK-deficient tumor-bearing mice, lack of type 1-associated cytokines correlates with the presence of type 2 (alternatively activated) monocytes and the production of type 2 cytokines. Furthermore these type 2 monocyte-containing splenic adherent populations potently suppress subsequent memory CTL restimulation. We evaluated the role of NK lytic effector functions in the efficient switch of the immune system toward classical (type 1) activation, by including differentially activated monocytic populations as targets in cytotoxicity assays. The results indicate that the accessory function of NK depend partially on the ability of activated NK cells to preferentially engage type 2 antigen presenting cells. Thus, when the immune system tends to be type 2-oriented, NK cells can drive an efficient type 2type 1 switch in the population of antigen presenting cells to provide signaling for the generation of CTLs. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? This article has been cited by other articles: J. Oberlies, C. Watzl, T. Giese, C. Luckner, P. Kropf, I. Muller, A. D. Ho, and M. Munder Regulation of NK Cell Function by Human Granulocyte Arginase J. Immunol., May 1, 2009; 182(9): 5259 - 5267. [Abstract] [Full Text] [PDF] A. Iannello, O. Debbeche, S. Samarani, and A. Ahmad Antiviral NK cell responses in HIV infection: I. NK cell receptor genes as determinants of HIV resistance and progression to AIDS J. Leukoc. Biol., July 1, 2008; 84(1): 1 - 26. [Abstract] [Full Text] [PDF] M. A. 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